Type 1 immunity enables neonatal thymic ILC1 production-Reference-Cited by-同舟云学术

Type 1 immunity enables neonatal thymic ILC1 production

Published:2024-01-19 Issue:3 Volume:10 Page:
ISSN:2375-2548
Container-title:Science Advances
language:en
Short-container-title:Sci. Adv.

Author:

Tougaard Peter¹²^ORCID,Pérez Mario R.¹²^ORCID,Steels Wolf¹²^ORCID,Huysentruyt Jelle¹²^ORCID,Verstraeten Bruno¹²^ORCID,Vetters Jessica³⁴^ORCID,Divert Tatyana¹²,Gonçalves Amanda²⁵^ORCID,Roelandt Ria¹²^ORCID,Takahashi Nozomi¹²^ORCID,Janssens Sophie³⁴^ORCID,Buus Terkild B.⁶^ORCID,Taghon Tom⁷⁸^ORCID,Leclercq Georges⁷⁸^ORCID,Vandenabeele Peter¹²^ORCID

Affiliation:

1. Cell death and Inflammation Unit, VIB-UGent Center for Inflammation Research, Ghent, Belgium.

2. Department of Biomedical Molecular Biology, Ghent University, Ghent, Belgium.

3. Laboratory for ER Stress and Inflammation, VIB Center for Inflammation Research, Ghent, Belgium.

4. Department of Internal Medicine and Pediatrics, Ghent University, Ghent, Belgium.

5. VIB BioImaging Core, VIB-UGent Center for Inflammation Research, Technologiepark-Zwijnaarde 71, Ghent 9052, Belgium.

6. LEO Foundation Skin Immunology Research Center, Department of Immunology and Microbiology, University of Copenhagen, Copenhagen, Denmark.

7. Department of Diagnostic Sciences, Ghent University, Ghent, Belgium.

8. Cancer Research Institute Ghent (CRIG), Ghent, Belgium.

Abstract

Acute thymic atrophy occurs following type 1 inflammatory conditions such as viral infection and sepsis, resulting in cell death and disruption of T cell development. However, the impact type 1 immunity has on thymic-resident innate lymphoid cells (ILCs) remains unclear. Single-cell RNA sequencing revealed neonatal thymic–resident type 1 ILCs (ILC1s) as a unique and immature subset compared to ILC1s in other primary lymphoid organs. Culturing murine neonatal thymic lobes with the type 1 cytokines interleukin-12 (IL-12) and IL-18 resulted in a rapid expansion and thymic egress of KLRG1 + CXCR6 + cytotoxic ILC1s. Live imaging showed the subcapsular thymic localization and exit of ILC1s following IL-12 + IL-18 stimulation. Similarly, murine cytomegalovirus infection in neonates resulted in thymic atrophy and subcapsular localization of thymic-resident ILC1s. Neonatal thymic grafting revealed that type 1 inflammation enhances the homing of cytokine-producing thymus-derived ILC1s to the liver and peritoneal cavity. Together, we show that type 1 immunity promotes the expansion and peripheral homing of thymic-derived ILC1s.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

Link

https://www.science.org/doi/pdf/10.1126/sciadv.adh5520

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